|Year : 2019 | Volume
| Issue : 1 | Page : 41-45
A controlled crossover study to assess the role of dietary eliminations in reducing the severity of atopic dermatitis in children
Pretty Mathew, Rajiv Sridharan, Thyvalappil Anoop, Ajayakumar Sreenivasan
Department of Dermatology, Pariyaram Medical College, Kannur, Kerala, India
|Date of Web Publication||14-Dec-2018|
Dr. Thyvalappil Anoop
Department of Dermatology, Pariyaram Medical College, Kannur - 670 503, Kerala
Source of Support: None, Conflict of Interest: None
Background: In the pathogenesis of atopic dermatitis (AD), immune sensitization to food-derived allergens has a role. However, the evidence of allergen sensitization is not a proof of clinically relevant allergy and it has to be confirmed by food challenges so that unnecessary food restrictions in growing children can be avoided. Aims and Objectives: This study was conducted to assess the clinical severity of AD in children after certain dietary modifications and to correlate absolute eosinophil count (AEC) with dietary modification. Materials and Methods: A total of thirty AD children were enrolled randomly into a trial period of egg and cow's milk exclusion diet or control period of egg and cow's milk inclusion diet of 3 weeks. At the end of 3 weeks, patients resumed their normal diet to minimize any carryover effect for next 3 weeks. In the last 3 weeks, the trial and the control groups were crossed over. Patients were assessed at baseline and at the end of each 3-week period using SCORing AD (SCORAD) index and AEC. The data were analyzed using paired t-test. Results: The mean SCORAD at the end of control and trial period was 18.3 and 14.3, respectively, with a mean difference of 3.4, which is statistically not significant (P = 0.165). The mean AEC at the end of control and trial period was 836.5 and 799.6, respectively, the reduction being statistically not significant. Conclusion: Our study could not confirm the beneficial effects of an allergen avoidance diet in AD. We propose that dietary elimination advices should be given only to patients with a definite history of food-induced exacerbations of the disease.
Keywords: Atopic dermatitis, dietary elimination, SCORing AD
|How to cite this article:|
Mathew P, Sridharan R, Anoop T, Sreenivasan A. A controlled crossover study to assess the role of dietary eliminations in reducing the severity of atopic dermatitis in children. Indian J Paediatr Dermatol 2019;20:41-5
|How to cite this URL:|
Mathew P, Sridharan R, Anoop T, Sreenivasan A. A controlled crossover study to assess the role of dietary eliminations in reducing the severity of atopic dermatitis in children. Indian J Paediatr Dermatol [serial online] 2019 [cited 2019 Jul 19];20:41-5. Available from: http://www.ijpd.in/text.asp?2019/20/1/41/247548
| Introduction|| |
Atopic dermatitis (AD) is a chronic, pruritic inflammatory skin disease that occurs most frequently in children but also in many adults. Food allergens may contribute to trigger and exacerbation of AD. Common food allergens include peanut, cow's milk, and egg white and rarely seafoods, soybean, and wheat. A careful clinical approach and parent education is the key to avoid unnecessary eliminations causing nutritional risk. In this study, children with AD were made to go through a short period of both food inclusion and elimination, and change in severity of AD and absolute eosinophil count (AEC) was assessed.
| Materials and Methods|| |
This was a hospital-based controlled crossover study, conducted in the department of dermatology, venereology, and leprology in a tertiary care center in North Kerala. Patients between 1 and 15 years' age group, with a diagnosis of AD according to Hanifin and Rajka criteria, were included in the study. Institutional ethical committee clearance was obtained. Patients who were on immune suppressants in the past 1 month, those with coexisting systemic disease, history of urticaria, or anaphylaxis to egg or milk, and those who do not take egg or milk are excluded from the study. After obtaining informed written consent, data were collected in pretested structured questionnaire along with relevant clinical examination including assessment of SCORing AD (SCORAD) index. SCORAD is a measurement of six clinical signs at a representative body site, along with surface area involvement and visual analog scales of pruritus and sleep loss to give a severity score of AD. Total duration of the study was 9 weeks.
The patients were enrolled randomly into trial period (egg and cow's milk exclusion diet) or control period (egg and cow's milk inclusion diet). Those patients in trial period were advised to avoid milk, egg, and all food items containing milk and egg for a period of 3 weeks. Patients in control period were advised to take egg and cow's milk (quantity adjusted according to the age of the patient) daily for the same duration. The next 3-week period patients resumed their normal diet to minimize any carryover effect. In the last 3-week period, the trial group and control group were crossed over.
The whole study population was advised to adhere to the treatment that they were receiving at the start of the study without any change. In case of severe flareups, they were excluded from the study and treated accordingly. Patients were assessed at baseline and at the end of each 3-week period using SCORAD index. AEC was also measured at the end of each 3-week period. The data thus obtained were analyzed using paired t-test.
| Results|| |
Thirty cases of AD were included in the study and were advised to follow certain dietary modifications. Majority (53.3%) of study population developed the disease below 10 months of age. Thirty percent of children reported age of onset of disease between 10 months and 18 months. Moreover, only 16.7% reported an onset above 1½ years. Majority were females (56.7%). A personal history of atopy was seen in 33.3% of children, 20% had a personal history of bronchial asthma (BA), and 20% elicited a personal history of allergic rhinitis.
All thirty children were taking cow's milk regularly. Eighty percent of the study population were in the habit of taking egg while 20% avoided eggs. History of food-induced exacerbation of AD was seen in 40% while rest 60% never noticed an exacerbation of AD related to food [Figure 1]. Out of 30 patients, 5 (16.7%) gave a history of exacerbation AD on taking both egg and prawns while 4 (13.3%) showed exacerbation with egg alone. About 6.7% showed exacerbation on taking fish other than prawns and 3.3% on taking prawns alone [Figure 2].
Family history of atopy was present in 80% of children. Nearly 33.3% of children had family history of AD. About 46.7% gave a family history of BA. Almost 53.3% showed a family history of allergic rhinitis.
Mean SCORAD at the baseline was 19.9, and at the end of trial period, it was 14.9. Mean difference was 5 and the difference was statistically significant (P = 0.042) [Table 1].
|Table 1: Comparison of SCORing Atopic Dermatitis at baseline and at the end of trial period|
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Mean SCORAD at the end of control period was 18.3, and at the end of trial period, it was 14.9. Mean difference was 3.4. Moreover, the difference was statistically not significant (P = 0.165) [Table 2].
|Table 2: Comparison of SCORing Atopic Dermatitis at the end of control period and at the end of trial period|
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Mean AEC at the end of control period was 836.5, while at the end of trial period, it was 799.6. Even though there was a reduction, it was not statistically significant [Table 3].
Mean AEC at the end of normal diet period was 822.0, and at the end of trial period, it was 799.6. The mean difference was not statistically significant [Table 4].
|Table 4: Comparison of absolute eosinophil count at the end of normal diet period and trial period|
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| Discussion|| |
A total of 30 children of 1–15 years old, diagnosed as AD according to Hanifin and Rajka criteria, were included in the study and were advised to follow certain dietary modification for the prescribed period. Majority (53.3%) of study population developed the disease below 10 months of age. Nearly 30.0% of children reported age of onset of disease between 10 months and 18 months and only 16.7% reported an onset above 1½ years.
In this study, majority were females (56.7%) with a female-to-male ratio of 1.31:1. Dhar et al., Sarkar and Kanwar, and Kaujalgi et al. reported a male predominance.,, Personal history of atopy was present in 33.3% of children, and allergic rhinitis (AR) and BA showed an equal prevalence of 20% each for the study population. Dhar et al. reported a personal history of atopy in 18.5% patients. In that, a history of AR was present in 12.3% and BA in 4.7%. Karthikeyan et al. showed a personal history of atopy in 15.37%.
In the present study, 80% had family history of atopy, which was much greater than the other studies. A family history of AD was seen in 33.3% of children, 46.7% gave a family history of BA, and 53.3% showed a family history of AR. Family history of atopy was present in 40% patients, 53.9% with BA, 19.2% each with AR and AD, and 5.8% in one study. Sarkar and Kanwar reported 36.37% and Karthikeyan et al. reported 35.35% children with family history of atopy.,
Food allergens may contribute to trigger and exacerbation of AD. AD is directly involved in the pathogenesis of food allergy rather than allergen-induced AD exacerbation. In young infants, AD is the main risk factor for food sensitization.
Food allergy can be immunoglobulin E (IgE)-mediated or non-IgE-mediated immunological reactions. Food allergy can appear immediate or late. Immediate reactions manifest as exacerbation of AD secondary to pruritus. Late reactions can occur after hours to 2 days of a trigger food as eczematous lesions. Food allergen-specific T-cells play a major role in the development of late eczematous responses and secondary scratching.
Subsidence of skin lesions and the time taken for resolution depend on the type of sensitizing food. When the sensitization is caused by egg white, milk, or wheat, lesions may disappear faster. Allergic reactions to nuts, fish, or seafood and the symptoms may persist even for the lifelong. Detailed history is essential for diagnosing food allergy. Serological tests, atopic patch tests, and food challenge tests are available for further confirmation.
All thirty children were taking cow's milk regularly. About 80% of the study population were in the habit of taking egg while 20% avoided eggs. Egg was avoided due to the fear of exacerbation of lesions. According to Manjra et al., it was even more, coming up to 60%. However, another study reported lesser values with 33% of patients with severe AD, 10%–20% with moderate AD, and 6% with mild AD showing food exacerbation. Another systematic review which supported a strong and dose-dependent association between food sensitization and food allergy showed increased severity, and chronicity of AD was associated with food allergy. This study also pointed out that AD precedes the development of food sensitization and allergy.
In the present study, 40% of patients gave a history of food-induced exacerbation of AD while rest 60% never noticed an exacerbation of AD related to food. Out of 30 patients, 5 (16.7%) gave a history of exacerbation AD on taking both egg and prawns while 4 (13.3%) showed exacerbation with egg alone. About 6.7% showed exacerbation on taking fish other than prawns and 3.3% on taking prawns alone. The most common food item exacerbating AD was egg followed by prawns. However, none of the children gave a definite history exacerbation with cow's milk probably due to the regular habit of cow's milk intake.
A Cochrane review of nine randomized controlled trials of food allergy in patients with AD showed that there appears to be no benefit of an egg and milk-free diet in unselected participants with atopic eczema. Only 2.2% had food aggravation of AD in a study by Upendra et al.
An open-pilot study conducted by Dhar et al. in which patients were advised to strictly adhere to a diet excluding milk and milk products, all kinds of nuts and nut-containing foods, egg and egg-containing foods, sea fish and prawns, brinjal, and soybean for a period of 3 weeks showed a statistically significant reduction in severity scores after dietary elimination alone.
There was statistically significant lowering of pruritus and sleeplessness as well as erythema, edema, crusting, and excoriations in another study on 148 AD patients, by following specific dietary eliminations for 3 weeks. Lichenification was not significantly reduced. Mild increase of SCORAD score was observed in 43 control patients with AD, who were not on this diet in the period of 3 weeks.
In the present study, the mean SCORAD at the baseline was 19.9, at the end of trial period, it was 14.9, and at the end of control period, it was 18.3. The SCORAD was reduced from a baseline mean of 19.9–14.9 at the end of trial period, and the difference is statistically significant (P = 0.042). There was no statitically signifant reduction in SCORAD at the end of trial period, compared to that at the end of control period. (P = 0.165). Two confusing results of the study noted were:
- Baseline value of SCORAD was greater than that of the allergen inclusion control period
- Even though comparison between baseline SCORAD and end of trial period SCORAD showed a significant reduction in severity of AD, the difference between SCORAD at the end of control and at the end of trial period failed to show a significant reduction in severity after adhering to cow's milk and egg-free period of 3 weeks. These findings may be attributed to the habit of regular intake of proposed allergens such as cow's milk and egg by majority of children.
Avoidance of a particular food should be advised only based on a clear history and diagnosis of food allergy. If there is consistent correlation of symptoms, a diagnostic elimination diet for up to 4–6 weeks with the suspected food item may be tried. If there is an improvement of the symptoms during a diagnostic elimination diet, an oral food challenge should be considered.
Dietary modification in cases of proven food allergy helps to decrease severity but does not replace the standard topical or systemic treatment of AD. Maintaining a food diary may help in identifying a specific food trigger. A double-blind placebo-controlled food challenge is the gold standard test to diagnose food allergies. If elimination diet is followed, these children should be supplemented with complementary foods rich in nutrients.
The greatest difficulty we faced during this study was the difficulty to implement a restrictive diet to the children even for a relatively short period of 3 weeks which resulted in reducing the sample size to thirty. Hence, we recommend further large-scale clinical trials to develop a consensus regarding dietary restrictions in AD, because blind dietary restrictions may lead to nutritional defi ciencies and growth retardations in children.
Dhar et al. and Krupa Shankar and Chakravarthi found a significant correlation between SCORAD and AEC., In the present study, we evaluated the effect of diet on AEC. Mean AEC at the end of control period was 836.5, while at the end of trial period, it was 799.6. Even though there is a small reduction in AEC at the end of trial period when compared to baseline and control period, the reduction was not statistically significant. Hence, the study concludes that dietary eliminations do not have a beneficial effect on AEC. Small sample size and less number of allergens included in the study were the limitations of our study. The inability to ensure specified quantity of allergen the patient has to take, during the allergen inclusion period, might also have influenced the results.
| Conclusion|| |
In this study, majority of patients were females. This study showed a higher incidence of personal and family history of atopy compared to other studies. Majority of patients do not have a history of food exacerbation of their AD. Most common food item resulting in exacerbation of lesions was egg followed by prawns. This study could not confirm the beneficial effect of an allergen avoidance diet in AD. Dietary modifications do not have any effect on AEC. We recommend further large-scale studies to confirm the effect of dietary restrictions in severity of AD.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Dhar S, Parikh D, Rammoorthy R, Srinivas S, Sarkar R, Inamadar A, et al
. Treatment guidelines for atopic dermatitis by ISPD Task Force 2016. Indian J Paediatr Dermatol 2017;18:174-6. [Full text]
Oszukowska M, Michalak I, Gutfreund K, Bienias W, Matych M, Szewczyk A, et al.
Role of primary and secondary prevention in atopic dermatitis. Postepy Dermatol Alergol 2015;32:409-20.
Spergel JM, Boguniewicz M, Schneider L, Hanifin JM, Paller AS, Eichenfield LF, et al.
Food allergy in infants with atopic dermatitis: Limitations of food-specific IgE measurements. Pediatrics 2015;136:e1530-8.
Tait C, Goldman RD. Dietary exclusion for childhood atopic dermatitis. Can Fam Physician 2015;61:609-11.
Hanifin JM, Rajka RG. Diagnostic features of atopic dermatitis. Acta Derm Venereol 1980;92:44-7.
Thakur A, Malhotra S, Malhotra S. Scoring atopic dermatitis and six sign atopic dermatitis: Comparison of prognostic and predictive value in atopic dermatitis. Indian J Paediatr Dermatol 2013;14:13-8. [Full text]
Dhar S, Malakar R, Banerjee R, Chakraborty S, Chakraborty J, Mukherjee S, et al.
An uncontrolled open pilot study to assess the role of dietary eliminations in reducing the severity of atopic dermatitis in infants and children. Indian J Dermatol 2009;54:183-5.
] [Full text]
Sarkar R, Kanwar AJ. Clinico-epidemiological profile and factors affecting severity of atopic dermatitis in North Indian children. Indian J Dermatol 2004;49:117-22. [Full text]
Kaujalgi R, Handa S, Jain A, Kanwar AJ. Ocular abnormalities in atopic dermatitis in Indian patients. Indian J Dermatol Venereol Leprol 2009;75:148-51.
] [Full text]
Karthikeyan K, Thappa DM, Jeevankumar B. Pattern of pediatric dermatoses in a referral center in South India. Indian Pediatr 2004;41:373-7.
Flohr C, Perkin M, Logan K, Marrs T, Radulovic S, Campbell LE, et al.
Atopic dermatitis and disease severity are the main risk factors for food sensitization in exclusively breastfed infants. J Invest Dermatol 2014;134:345-50.
Katta R, Schlichte M. Diet and dermatitis: Food triggers. J Clin Aesthet Dermatol 2014;7:30-6.
Celakovská J, Karel E, Jaroslava V, Ettlerová K. Allergy to soy in an adolescent suffering from atopic dermatitis. Indian J Dermatol 2013;58:247.
Manjra AI, du Plessis P, Weiss R, Motala CM, Potter PC, Raboobee N, et al.
Childhood atopic eczema consensus document. S Afr Med J 2005;95:435-40.
Forbes LR, Saltzman RW, Spergel JM. Food allergies and atopic dermatitis: Differentiating myth from reality. Pediatr Ann 2009;38:84-90.
Tsakok T, Marrs T, Mohsin M, Baron S, du Toit G, Till S, et al.
Does atopic dermatitis cause food allergy? A systematic review. J Allergy Clin Immunol 2016;137:1071-8.
Bath-Hextall F, Delamere FM, Williams HC. Dietary exclusions for established atopic eczema. Cochrane Database Syst Rev 2008;(1):CD005203.
Upendra Y, Keswani N, Sendur S, Pallava A. The clinico-epidemiological profile of atopic dermatitis in residential schoolchildren: A study from South Chhattisgarh, India. Indian J Paediatr Dermatol 2017;18:281-5. [Full text]
Dhar S, Banerjee R. Atopic dermatitis in infants and children in India. Indian J Dermatol Venereol Leprol 2010;76:504-13.
] [Full text]
Celakovská J, Bukač J. Hypoallergenic diet can influence the severity of atopic dermatitis. Indian J Dermatol 2013;58:239.
Criton S, Gangadharan G. Non pharmacological management of atopic dermatitis. Indian J Paediatr Dermatol 2017;18:166-73. [Full text]
Dhar S, Parikh D, Rammoorthy R, Srinivas S, Sarkar R, Inamadar A, et al
. Maternal dietary antigen avoidance during pregnancy or lactation. Indian J Paediatr Dermatol 2017;18:181-2. [Full text]
Dhar S, Srinivas SM. Food allergy in atopic dermatitis. Indian J Dermatol 2016;61:645-8.
] [Full text]
Dhar S, Mondal B, Malakar R, Ghosh A, Gupta AB. Correlation of the severity of atopic dermatitis with growth retardation in pediatric age group. Indian J Dermatol 2005;50:125-8. [Full text]
Krupa Shankar DS, Chakravarthi M. Atopic patch testing. Indian J Dermatol Venereol Leprol 2008;74:467-70.
] [Full text]
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4]